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Prenatal diethylstilbestrol exposure and risk of diabetes, gallbladder disease, and pancreatic disorders and malignancies
- Rebecca Troisi, Marianne Hyer, Linda Titus, Julie R. Palmer, Elizabeth E. Hatch, Dezheng Huo, Kjersti M. Aagaard, William C. Strohsnitter, Robert N. Hoover
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- Journal:
- Journal of Developmental Origins of Health and Disease / Volume 12 / Issue 4 / August 2021
- Published online by Cambridge University Press:
- 28 October 2020, pp. 619-626
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- Article
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Prenatal diethylstilbestrol (DES) exposure is associated with increased risk of hormonally mediated cancers and other medical conditions. We evaluated the association between DES and risk of pancreatic cancer and pancreatic disorders, type 2 diabetes, and gallbladder disease, which may be involved with this malignancy. Our analyses used follow-up data from the US National Cancer Institute DES Combined Cohort Study. Cox proportional hazards models estimated hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for age, sex, cohort, body mass index, smoking, and alcohol for the association between prenatal DES exposure and type 2 diabetes, gallbladder disease (mainly cholelithiasis), pancreatic disorders (mainly pancreatitis), and pancreatic cancer among 5667 exposed and 3315 unexposed individuals followed from 1990 to 2017. Standardized incidence rate (SIR) ratios for pancreatic cancer were based on age-, race-, and calendar year-specific general population cancer incidence rates. In women and men combined, the hazards for total pancreatic disorders and pancreatitis were greater in the prenatally DES exposed than the unexposed (HR = 11, 95% CI 2.6–51 and HR = 7.0, 95% CI 1.5–33, respectively). DES was not associated overall with gallbladder disease (HR = 1.2, 95% CI 0.88–1.5) or diabetes (HR = 1.1, 95% CI 0.9–1.2). In women, but not in men, DES exposure was associated with increased risk of pancreatic cancer compared with the unexposed (HR: 4.1, 95% CI 0.84–20) or general population (SIR: 1.9, 95% CI 1.0–3.2). Prenatal DES exposure may increase the risk of pancreatic disorders, including pancreatitis in women and men. The data suggested elevated pancreatic cancer risk in DES-exposed women, but not in exposed men.
Contributors
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- By Magdalena Anitescu, Charles E. Argoff, Arash Asher, Nyla Azam, Nomen Azeem, Sachin K. Bansal, Jose E. Barreto, Rodrigo A Benavides, Niteesh Bharara, Justin B. Boge, Robert B. Bolash, Thomas K. Bond, Christopher Centeno, Zachariah W. Chambers, Jonathan Chang, Grace Chen, Hamilton Chen, Jeffry Chen, Jianguo Cheng, Natalia Covarrubias, Claire J. Creutzfeldt, Gulshan Doulatram, Amirpasha Ehsan, Ike Eriator, Jeff Ericksen, Mark Etscheidt, Frank J. E. Falco, Jack Fu, Timothy Furnish, Annemarie E. Gallagher, Kingsuk Ganguly, Eugene Garvin, Cliff Gevirtz, Scott E. Glaser, Brandon J. Goff, Harry J. Gould, Christine Greco, Jay S. Grider, Maged Guirguis, Qiao Guo, Justin Hata, John Hau, Garett J. Helber, Eric R. Helm, Lori Hill Marshall, Dean Hommer, Jeffrey Hopcian, Eric S. Hsu, Jakun Ing, Tracy P. Jackson, Gaurav Jain, Chrystina Jeter, Alan David Kaye, James Kelly, Soorena Khojasteh, Ankur Khosla, Daniel Krashin, Monika A. Krzyzek, Prasad Lakshminarasimhiah, Steven Michael Lampert, Garrett LaSalle, Quan D. Le, Ankit Maheshwari, Edward R. Mariano, Joaquin Maury, John P. McCallin, John Michels, Natalia Murinova, Narendren Narayanasamy, Rebekah L. Nilson, Elliot Palmer, Vikram B. Patel, Devin Peck, Donald B. Penzien, Danielle Perret Karimi, Tilak Raj, Michael R. Rasmussen, Mohit Rastogi, Rahul Rastogi, Nashaat N. Rizk, Rinoo V. Shah, Paul A. Sloan, Julian Sosner, A. Raj Swain, Minyi Tan, Natacha Telusca, Santhosh A. Thomas, Andrea Trescot, Michael Truong, Jason Tucker, Richard D. Urman, Brandon A. Van Noord, Nihir Waghela, Irene Wu, Jiang Wu, Jijun Xu, Jinghui Xie, William Yancey
- Edited by Alan David Kaye, Louisiana State University, Rinoo V. Shah
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- Book:
- Case Studies in Pain Management
- Published online:
- 05 October 2014
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- 16 October 2014, pp xi-xv
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Contributors
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- By Louise B. Andrew, Jane C. Ballantyne, Sadek Beloucif, David Clendenin, Maliha A. Darugar, Joanna M. Davies, Michael DeVita, Denise M. Dudzinski, Bernice Elger, Monica Escher, Joel E Frader, Kelly Fryer-Edwards, James Giordano, Allen Gustin, Rebecca M. Harris, Gerhard Höver, Steven K. Howard, Carl C. Hug, Samia Hurst, Steven Jackson, Nancy S. Jecker, Jonathan D Katz, Joseph Klein, W. Andrew Kofke, Ruth Landau, Craig D. McClain MD, Alex Mauron, Kelly N. Michelson, Cynthiane J. Morgenweck, William Notcutt, Michael Nurok, Susan K. Palmer, Joan G. Quaine, Michael A. Rie, Stanley H. Rosenbaum, David M. Rothenberg, Robert B. Schonberger, Mark D. Siegel, Jeffrey H. Silverstein, Murali Sivarajan, Karen Souter MD, Thomas Specht MD, Andrea Trescot, Gail A. Van Norman, A.M. Viens, Elizabeth K. Vig, David B. Waisel, Clarence Ward, James M. West, Richard L Wolman, Steve Yentis
- Edited by Gail A. Van Norman, University of Washington, Stephen Jackson, Stanley H. Rosenbaum, Susan K. Palmer
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- Book:
- Clinical Ethics in Anesthesiology
- Published online:
- 05 March 2012
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- 28 October 2010, pp xi-xiv
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Coaggregation and coadhesion in oral biofilms
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- By Pual E. Kolenbrander, Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA, Roxanna N. Andersen, Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA, Karen M. Kazmerzak, Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA, Robert J. Palmer, Jr, Oral Infection and Immunity Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892, USA
- Edited by David G. Allison, University of Manchester, P. Gilbert, University of Manchester, H. M. Lappin-Scott, University of Exeter, M. Wilson
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- Book:
- Community Structure and Co-operation in Biofilms
- Published online:
- 03 June 2010
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- 23 October 2000, pp 65-86
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Summary
COAGGREGATION AND COADHESION
Certain molecules on the surfaces of human oral bacteria can be recognized by cognate surface components of genetically distinct cells, which bind to form networks of cell–cell interactions. When these interactions occur in suspension, they are called coaggregations (Kolenbrander, 1988). When the interaction occurs between suspended or planktonic cells and already adherent cells, it is called coadhesion (Bos et al., 1994). Coadhesion may involve the accretion of an already formed coaggregate onto a biofilm, which is an assemblage of living cells on a substratum, or onto a virgin surface.
Coaggregation among human oral bacteria was first described 30 years ago (Gibbons & Nygaard, 1970). Coaggregation is measured by several methods, including visual inspection of clumps or coaggregates after mixing dense suspensions of two cell types (Gibbons & Nygaard, 1970), turbidometric measurement of supernatant after slowspeed centrifugation to pellet the coaggregates (McIntire et al., 1978), filtration through specific pore size to separate single cells from coaggregates (Lancy et al., 1980), distribution of radiolabelled cells of one cell type in coaggregates and supernatant after slow-speed centrifugation (Kolenbrander & Andersen, 1986) and binding of a radiolabelled cell type to partner cells immobilized on a nitrocellulose membrane (Lamont & Rosan, 1990). Coaggregations may be unimodal or bimodal (Kolenbrander, 1997). Unimodal coaggregations involve protease-sensitive molecules on the cell surface of one of the partners recognizing their cognate receptors (protease-insensitive) on the other partner's cell surface. Bimodal coaggregations involve more than one of the unimodal mechanisms. For example, one partner expresses both an adhesin and a non-cognate receptor. Its partner expresses the respective cognates for the adhesin and receptor.
Nafcillin Resistant Staphylococcus Aureus A Possible Community Origin
- Ayser C. Hamoudi, Robert N. Palmer, Timothy L King
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- Journal:
- Infection Control / Volume 4 / Issue 3 / May/June 1983
- Published online by Cambridge University Press:
- 02 January 2015, pp. 153-157
- Print publication:
- May/June 1983
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An increased incidence in nafcillin (semisynthetic penicillins) resistant Staphylococcus aureus (SR-SA), which peaked in January 1980, was noted in Columbus Children's Hospital (CCH), Columbus, Ohio. To investigate the source of this outbreak, we reviewed the susceptibility patterns of S. aureus strains isolated at CCH for a 12-month period (July 1979 to June 1980). A total of 773 isolates from 706 patients were investigated with a total of 40 patients colonized or infected with SR-SA, approximately 25% of which were diagnosed in the ambulatory clinics. These patients did not have any apparent previous contact with the inpatient unit or inpatient personnel. Eight nosocomial infections were also uncovered. The first appeared in December 1979. Our studies suggested that some SR-SA isolates may have originated in the community and these organisms may not be exclusive to the hospital environment, as was felt to be the case previously. We also determined that the baseline incidence for our hospital of SR-SA was approximately 2% of total S. aureus isolates. Only 35% of the SR-SA demonstrated resistance to multiple antibiotics. This report indicates that community and nosocomial 5. aureus isolates should be monitored for nafcillin resistance. Vancomycin susceptibility should be tested on all isolates and reported for SR-SA in life-threatening infections.